WordNet

to put down by force or authority; "suppress a nascent uprising"; "stamp down on littering"; "conquer ones desires" (同)stamp down, inhibit, subdue, conquer, curb
reduce the incidence or severity of or stop; "suppress a yawn"; "this drug can suppress the hemorrhage"
put out of ones consciousness (同)repress
an electrical device for suppressing unwanted currents (同)suppresser
someone who suppresses; "dictators are suppressors of free speech" (同)suppresser
a gene that suppresses the phenotypic expression of another gene (especially of a mutant gene) (同)suppresser, suppressor_gene, suppresser gene
(genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
the spreading of a disease (especially cancer) to another part of the body
informal term for information; "give me the gen on your new line of computers"

PrepTutorEJDIC

〈反乱など〉‘を'『鎮圧する』…,‘の'活動を押える / 〈感情・欲望など〉‘を'『抑制する』,抑える / …‘の'発表を禁止する,伏せる
抑圧する人,鎮圧者 / (ラジオ・テレビの)妨害電波(混信)防止装置
遺伝子
(癌(がん)などの)転移

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/12/02 00:46:52」(JST)

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[Wiki en表示]

A metastasis suppressor is a protein that acts to slow or prevent metastases (secondary tumors) from spreading in the body of an organism with cancer. Metastasis is one of the most lethal attributes of cancer. This attribute is responsible for about ninety percent of human cancer deaths.^[1] These proteins that act to slow or prevent metastases are different from ones that act to suppress tumor growth. Genes for about a dozen such proteins are known in humans and other animals.^[2]

Background

The treatment of cancer has usually been aimed at destroying the primary tumor or at least in stopping its growth. Even though major improvements in the methods of surgery, radiation, and chemotherapy have taken place, often enough there have not been corresponding improvements in patient survival. Treatment methods that focus on the primary cancer typically fall short in aiding the patient after the cancer has metastasized.^[1]

Metastasis suppressors act by different mechanisms than tumor suppressors, and they have no effect on primary tumors. Tumor suppressors, however, also block metastasis, since metastasis is dependent upon tumorigenicity.^[1]

Eight metastasis suppressors have been identified, and most act by altering aspects of signal transduction. NM23 is a suppressor active in melanoma, breast and colon cancers, and apparently inhibits the functioning of a kinase enzyme that promotes cell division. MKK4 is a suppressor active in prostate and ovarian cancers, and apparently functions by facilitating apoptosis, or death of abnormal cells such as cancer cells. KAI1 is found in prostate and breast cancers, and forms complexes with proteins called integrins. Integrins are one of the structures that link cells together, and the complex formation may inhibit detachment and migration of the cancer cells. BRMS1 promotes the activity of the gap junctions of cells. The gap junctions are found on the cell membranes and allow for chemical and electrical communication between cells. It has been proposed that this communication between metastic tumor cells might contribute to inhibition of metastic growth. KISS1 is found in melanoma and breast cancers, and acts by synthesizing a protein receptor. RHOGD12 is active in bladder cancer, and inhibits proteins that aid in cancer cell migration. CRSP3 and VDUP1 are both active in melanoma. CRSP3 is a co-activator of genes involved in cancer growth, while VDUP1 inhibits a protein involved in cell proliferation.^[1]

Impact

Metastasis suppressor genes may offer valuable mechanistic insight for guiding specific therapeutic strategies, which may include drug-induced reactivation of metastasis suppressor genes and their signaling pathways. Clinical assessment of metastasis suppressor gene product status in disseminated cancer cells may improve the accuracy of predicting the prognosis in patients with clinically localized disease.^[3] Before any new treatments are implemented for general use, doctors conduct studies to find out whether the treatment is both safe for patients and effective against the disease. The results of such studies will ultimately provide the answers needed to continue work on antimetastasis drug development. Future studies should however, focus on treatment at the secondary tumor sites. This is a method to make progress in fighting cancer.^[2] These proteins are different from ones that act to suppress tumor growth.^[4] Genes for about a dozen such proteins are known in humans and other animals, including BRMS1, CRSP3, DRG1, KAI1, KISS1, NM23, and various TIMPs.^[5]^[6]

References

^ ^a ^b ^c ^d Olle, David (September 9, 2009). "Metastasis Suppressors". Suite 101. Missing or empty |url= (help)^{[self-published source?]}
^ ^a ^b Sobel, Mark E. (1990). "Metastasis Suppressor Genes". Journal of the National Cancer Institute 82 (4): 267–76. doi:10.1093/jnci/82.4.267. PMID 2405170.
^ Kauffman, Eric C.; Robinson, Victoria L.; Stadler, Walter M.; Sokoloff, Mitchell H.; Rinker-Schaeffer, Carrie W. (2003). "Metastasis Suppression: The Evolving Role of Metastasis Suppressor Genes for Regulating Cancer Cell Growth at the Secondary Site". The Journal of Urology 169 (3): 1122–33. doi:10.1097/01.ju.0000051580.89109.4b. PMID 12576866.
^ Yoshida, Barbara A.; Sokoloff, Mitchell M.; Welch, Danny R.; Rinker-Schaeffer, Carrie W. (2000). "Metastasis-Suppressor Genes: a Review and Perspective on an Emerging Field". Journal of the National Cancer Institute 92 (21): 1717–30. doi:10.1093/jnci/92.21.1717. PMID 11058615.
^ Shevde, Lalita A.; Welch, Danny R. (2003). "Metastasis suppressor pathways—an evolving paradigm". Cancer Letters 198 (1): 1–20. doi:10.1016/S0304-3835(03)00304-5. PMID 12893425.
^ Jackson, Paul, ed. (2007). New Developments in Metastasis Suppressor Research. New York: Nova Science Publishers. ISBN 978-1-60021-603-9. ^{[page needed]}

UpToDate Contents

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1. 前立腺癌の分子生物学 molecular biology of prostate cancer
2. 大腸癌の病理および予後決定因子 pathology and prognostic determinants of colorectal cancer
3. 乳癌における予後因子の評価 measurement of prognostic factors in breast cancer

English Journal

Frequent deletion of 3p21.1 region carrying semaphorin 3G and aberrant expression of the genes participating in semaphorin signaling in the epithelioid type of malignant mesothelioma cells.

Yoshikawa Y, Sato A, Tsujimura T, Morinaga T, Fukuoka K, Yamada S, Murakami A, Kondo N, Matsumoto S, Okumura Y, Tanaka F, Hasegawa S, Hashimoto-Tamaoki T, Nakano T.SourceDepartment of Genetics, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
International journal of oncology.Int J Oncol.2011 Dec;39(6):1365-74. doi: 10.3892/ijo.2011.1158. Epub 2011 Aug 12.
Array-based comparative genomic hybridization analysis was performed on 21 malignant mesothelioma (MM) samples (16 primary cell cultures and 5 cell lines) and two reactive mesothelial hyperplasia (RM) primary cell cultures. The RM samples did not have any genomic losses or gains. In MM samples, dele
PMID 21842119

Metastatic suppressor CD44 is related with oxidative stress in breast cancer cell lines.

Echiburu-Chau C, Roy D, Calaf GM.SourceInstituto de Alta Investigacion, Universidad de Tarapaca, Arica, Chile.
International journal of oncology.Int J Oncol.2011 Dec;39(6):1481-9. doi: 10.3892/ijo.2011.1154. Epub 2011 Aug 9.
Evidence has accumulated on the role of reactive oxygen species (ROS) in metastasis since surgical removal of tumors generates oxidative stress promoting metastasis and cell growth. Metastasis consists of a cascade of events which allow the cell to survive in target tissues and influence several pro
PMID 21833471

Japanese Journal

肺癌を合併したリンパ脈管筋腫症の2例におけるTSC 遺伝子異常の検討

澤田貴裕,林大久生,熊坂利夫,武内健一,平野春人,大浦裕之,半田政志,冨地信和,小野貞英
肺癌 51(3), 193-201, 2011
背景．リンパ脈管筋腫症（LAM）は腫瘍抑制遺伝子TSC の異常によって発症し，リンパ管の新生能を有することが知られている．肺癌を合併するLAMは稀である．症例．症例1：64歳，女性．右上肺野に腫瘤影を指摘され，また両肺に多発性嚢胞陰影がみられた．切除肺組織では，右S1?S3の肺癌（腺癌）と2群リンパ節に転移を認めた．また，多発性嚢胞性病変はLAMと診断された．さらに，微小結節性肺胞上皮過形成（MM …
NAID 130000761273

神経線維腫症I型(von Recklinghausen 病)に合併した鼻腔平滑筋肉腫例

尾上義浩,小池修治,那須隆,野田大介,石田晃弘,石井健一,青柳優
耳鼻咽喉科臨床 102(11), 931-937, 2009-11-01
… The patient was discharged without postsurgical treatment and is being followed up, showing no recurrence or metastasis as of this writing. … The risk of malignancy among NF1 patients is higher than among the general population, i.e., the NF1 gene is a tumor suppressor gene of which mutation involves a fourfold increased risk for cancer. …
NAID 10025527376

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★リンクテーブル★

リンク元	「antioncogene」「cancer suppressor gene」「growth suppressor gene」「転移抑制遺伝子」
関連記事	「suppress」「suppressor」「metastasis」